Dr. Julie, a.k.a. Scientific Chick, brings you insights into what's happening in the world of life sciences. Straight from the scientific source, relevant information you should know about, in plain language.

Sunday, October 31, 2010

When I picked my paper for this week’s blog, a very recent article published in PNAS, I didn’t factor in that I would write it on Halloween. Now I realize it’s going to seem like some cruel joke: on the one night where people stay up late walking the streets with flashlights and eat candies, I’m writing about the link between light at night and obesity. Wow. If I had tried to pick something more fitting, I couldn’t have done a better job.

We all know obesity is on the rise and there are several reasons to explain the epidemic: increased intake of calories (Double Down sandwich, anyone?), dietary choices (cheezy poofs instead of apples, anyone?) and lack of exercise (reading blogs, anyone?). However, the rise of obesity rates also coincides with an increase in light at night – the artificial lighting that allows us to write blogs late at night and catch up on all other activities we didn’t have time to do during the daytime. The problem is that light is closely tied to our circadian rhythm (the built-in clock that controls our biological processes and our behaviour). When our circadian rhythm is disrupted (an extreme example of this is shift workers), so is our metabolism. Based on this logic, an international team of researchers set out to test whether light at night plays a role in the weight of mice.

The researchers divided their mice into three groups. The control group was housed in the standard light/dark cycle. Another group of mice was housed in a light/dim light cycle (let’s call them the “dim” group). Finally, a third group of mice was housed in a continuously lit room (let’s call them the “bright” group). The mice were housed in these conditions for eight weeks, and during this time, the researchers monitored a number of parameters including body mass, food intake, activity levels, and glucose tolerance (how quickly sugar is cleared from the blood).

The researchers found that all the mice that experienced light at night (both the dim group and the bright group) got significantly fatter than the control mice. What’s more, the dim group and the bright group also exhibited impaired glucose tolerance (this can mean the mice are in a prediabetic-like state). Did the light at night groups of mice eat more (who doesn’t get the munchies when watching a late-night movie)? No. Did they exercise less (who goes for a run at midnight)? Also no. So what happened?

As it turns out, while the two light at night groups of mice ate just as much as the control mice, they ate at different times. Mice are nocturnal animals, and so normally they do most of their eating at night. The mice in the dim group, however, ended up eating over half of their food during the “light” phase. When the mice in the dim group were forced to eat their normal food intake only during the normal (dark) time, they didn’t gain weight. How crazy is that? These results suggest that light at night disrupts the timing of food intake, and this throws the metabolism out of whack.

Anyone who has looked up weight loss tips knows that it’s a good habit to forgo eating past a certain time of night (usually 7 or 8pm) if you want to lose weight. The reason usually given to explain this is that night time food is most often unhealthy and calorie-laden snacks: munchies during a movie, or ice cream after a distressing phone call from the ex-boyfriend. This study suggests there might be something more to this weight loss strategy: it may be all about listening to our biological clock.

Sunday, October 24, 2010

Last week, I wrote about how walking can protect your brain against cognitive decline. Sounds easy, right? The truth is, there are several factors that impact brain health, and exercise is just one of them. This week, I'm going way back in time to 2007 to look at a different way to keep your brain healthy: apprendre une autre langue.

Canadian researchers were interested in the relationship between bilingualism and Alzheimer's disease. Their hypothesis was based on the concept of cognitive reserve, a term that represents the attributes of your brain that make it resistant to damage. For example, you might have heard that keeping your mind challenged by doing crossword puzzles can delay cognitive decline. This is one way to increase your cognitive reserve. Presumably, complex mental activity like crossword puzzles but also like speaking more than one language can lead to a lesser chance of developing dementia and, in the event where you do get dementia, a slower rate of decline.

The researchers sifted through the records of over 200 patients from a memory clinic. About half of their sample spoke one language and half spoke two languages. The researchers assessed the relationship between the number of languages each patient spoke and whether each patient had Alzheimer's disease. For the patients who did have Alzheimer's disease, the researchers noted how old the person was when the disease started. Of course, the researchers controlled their results for all the obvious potential biases, such as cultural differences, immigration, formal education and employment status.

The results of this analysis show that the bilingual patients developed Alzheimer's disease much later (4.1 years on average) than the monolingual patients. Since developing an age-associated disease like Alzheimer's later means you have a greater chance of dying before you get the disease, delaying the onset by 4 years means a reduction in the total cases of Alzheimer's disease. Currently, no drugs have an effect that's comparable to bilingualism.

Since no study is ever perfect, let me point out two small caveats before you fish out your old high school Spanish books. First, there is one thing the researchers could not control for, and that is whether cultural differences could lead to delays in seeking medical help for a condition. This could muck up the results because if some patients delayed their first medical visit, then the age at which they received the diagnosis for Alzheimer's disease could be skewed. Second, the protective effect of speaking two languages cannot be generalized to people who have some knowledge of another language but are not fully bilingual. In this study, the patients who were bilingual were true bilinguals, fluent in both languages and having used both languages regularly for most of their lives.

Still, it's a good reminder that a busy mind is a healthy mind. And it's nice to have evidence to justify the occasional weekend in Paris.

Reference: Bilingualism as a protection against the onset of symptoms of dementia. (2007) Bialystok E et al. Neuropsychologia 45:459-464.

Sunday, October 17, 2010

It's no secret that exercising is key to maintaining a healthy brain as we get older. We hear it all the time. So why isn't everybody exercising? After all, it represents a form of personal health insurance, and it's way cheaper than Sun Life. The truth is, even though many people are aware that exercising is good for them, they are not compelled to change their lifestyle because it's not exactly clear what kind of exercise is best, how long you need to do it, and what exactly it does to help your brain. Well, I'm going to tell you.

In a recent study published in the journal Neurology, American researchers looked at 299 adults with a mean age of 78 years old. They evaluated how active each person was by measuring how many blocks they walked over the period of one week (this ranged between zero and 300!). The researchers then waited nine years (!), and then took brain images for all the participants and evaluated their level of cognitive impairment.

Not surprisingly, the more someone walked, the greater their brain volume after nine years. Greater amounts of physical activity predicted bigger volumes for several brain regions associated with thinking and memory, such as the hippocampus and the frontal cortex. What's more, the bigger brains associated with physical activity cut the risk for cognitive impairment in half.

The magic number in this study is 72. Walking a minimum of 72 blocks per week was necessary to see the bigger brain effect. Walking more than 72 blocks didn't lead to an even bigger brain. While I wouldn't necessarily shoot for walking only and exactly 72 blocks per week (as physical activity is also associated with a decreased risk for some illnesses), it's nice to have a baseline number, and to know that an exercise as simple as walking can make a difference.

Sunday, October 10, 2010

Almost one year ago, I wrote a post on optogenetics, a new field that combines optical techniques (playing with light) and genetic techniques (playing with DNA) to study the brain. Optogenetics is an extremely powerful technique that can be used to control the activity of brain cells. So far, it’s been mostly researched as an experimental tool, but a recent study published in the journal Nature hints at the possibility of using this technique to learn how to treat the most common neurodegenerative disorder after Alzheimer’s disease: Parkinson’s.

Parkinson’s disease, a movement disorder, affects a part of the brain called the basal ganglia, which is critical for planning movement and selecting appropriate actions. The basal ganglia can be roughly divided into two pathways (or networks of brain cells): a “direct” pathway that facilitates (or enables) movement and an “indirect” pathway that inhibits (or prevents) movement. When someone has Parkinson’s disease, it is thought that their direct pathway is not active enough and that their indirect pathway is too active, and this leads to the muscle rigidity, tremors and slowing of physical movement.

In this study, the researchers used a virus to deliver a special channel to the brain cells of either the direct or the indirect pathway of the basal ganglia in mice. This may sound confusing at first, but it’s a really clever experiment. Here is how it works: when certain types of viruses infect cells, they incorporate their DNA into the DNA of the “host” cell, such that the host starts making virus DNA, and ultimately turns into a virus-making factory. The researchers essentially hijacked this process: they engineered a virus that contained the DNA for the special channel, and therefore, once the brain cells got infected, they started making the special channel. What’s so special about this channel? It is activated by light (hence the “opto” in “optogenetics”). When blue light hits this channel, it activates the brain cells.

To tease out the differences between the direct and the indirect pathways, the researchers divided their mice into three groups: a control group (no brain cells infected with the virus), a “direct” group (the virus targets the direct pathway, such that only cells in the direct pathway have the special channel), and an “indirect” group (the virus targets the indirect pathway, such that only cells in the indirect pathway have the special channel). By exploiting this technique, the researchers were able to activate either the direct pathway or the indirect pathway of the basal ganglia simply by shining blue light onto the brain of the mice.

(I realize this is all very complicated, but if you’re still with me at this point, congratulations on completing Optogenetics 101!)

And now for the results… *drumroll* As expected, when the direct pathway was activated, the mice moved more (they ran around more, stood up on their hind legs more, etc.). And when the indirect pathway was activated, the mice froze, and overall moved less. How’s this for mind control?

At this point, it’s easy to get carried away and imagine a plethora of crazy scenarios should this technology fall in the hands of the bad guys (“And now, you will dance for me! Gnahahaha!”) However, the researchers had good intentions. They went on to activate the direct pathway in a mouse model of Parkinson’s disease, and found that this procedure rescued the locomotion deficits of the mice. And that is a wicked finding.

Unfortunately, treating humans with optogenetics is not going to happen anytime soon. There are significant hurdles to overcome before we can even think about it: working with viruses in the brain, delivering the channels only where we want them, assessing unwanted effects, and so on. That said, this study elegantly confirms that somehow activating the basal ganglia’s direct pathway could be an important therapeutic target to treat Parkinson’s disease.

Sunday, October 3, 2010

With all the discussions around climate change, it's no surprise that researchers are increasingly studying the impact of human activity on the environment. This type of research can take many forms ranging from the effects of city lights on the migratory paths of birds to the composition of soil in traditional and organic farming. Beyond research, climate change and other environmental discussions have also changed how we (or at least some of us) act at home. We try to remember to shut the lights. We take shorter showers. We recycle. But there's one sneaky way in which most of us impact the environment, sometimes on a daily basis, without ever thinking about it: when we swallow pills.

Most pharmaceutical drugs, from regular pain killers to chemotherapy drugs, are not fully processed by the body. This means that we end up excreting a proportion of the drugs we swallow, or by-products of those drugs. This leftover pharmaceutical trash ends up in sewage, and eventually makes its way into our aquatic systems.

A recent study by Canadian researchers looked at how low and high concentrations of Prozac, the popular antidepressant, affects the reproductive systems of the goldfish. The news are not good. The researchers found that even low concentrations of Prozac, similar to what could exist in the environment, significantly decreased the volume of sperm the fish produced when they were sexually stimulated. At the rate we're going, we're going to need to feed our fish Viagra to compensate for their antidepressant load.

I wrote a story on this study for The Mark, a Canadian online forum of news, commentaries and debate. You can read the full article here.

About Me

Dr. Julie is an Assistant Professor of Neurology at the National Core for Neuroethics and the Djavad Mowafaghian Centre for Brain Health at the University of British Columbia. She holds a PhD in Neuroscience.